[Neonatal necrotizing enterocolitis: nutritional care for surgical patients].
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A retrospective study comparing 16 full-term and 18 pre-term neonates with NEC operated on at Siriraj Hospital between 1987 and 1999 is presented. Major risk factors leading to NEC in full-term neonates included sepsis, SGA, birth asphyxia, severe jaundice requiring exchange transfusion and chorioamnionitis. Although full-term neonates developed NEC earlier than pre-term neonates (8.56 days vs 12.78 days), the average ages of operation in both groups were the same. There was no difference in CBC and bacteriological culture's results between term and pre-term patients. The decision to conduct operative treatments for full-term neonates with NEC was mostly based on only clinical signs of peritonitis (56.25%) before the pneumoperitoneum developed (31.25%). Ileo-caecal region was the most common site of bowel necrosis in both premature and full-term infants. Although term infants had a better 3-month survival rate than pre-term neonates (75% and 61% respectively), both groups had the same surgical complication rates.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
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We reviewed pathology specimens from 84 patients seen during a 10-year period with neonatal necrotizing enterocolitis, and these findings were correlated with clinical features. Coagulation (ischemic) necrosis, inflammation, and bacterial overgrowth were all present in the intestine of nearly all patients but with individual variability in the severity of these findings. Overall, coagulation necrosis was more severe than any other finding in most infants, indicating the importance of ischemia in the pathophysiology of necrotizing enterocolitis. Reparative tissue changes such as epithelial regeneration, granulation tissue formation, and fibrosis, found in two thirds of cases, suggested ongoing tissue injury of at least several days' duration. Birth weight, Apgar score, age, feeding status, and the presence of respiratory distress syndrome were not correlated with any particular histologic feature. The pathologic changes of necrotizing enterocolitis suggest that its cause is multifactorial, with ischemia, inflammation, bacterial overgrowth, and reparative tissue changes all playing important roles.
Fourteen infants with intestinal stenosis as a late sequela of necrotizing enterocolitis were treated at Texas Children's and Ben Taub General Hospitals from 1972 to 1979. Barium enema studies are the keystone in making the diagnosis and should be performed in any infant with abdominal distention or poor feeding after recovery from acute necrotizing enterocolitis. Spontaneous resolution of stenosis is a definite clinical entity, and nonobstructed infants should be given a trial for resolution. This trial should be for a limited time. The operative therapy for the infant with obstruction or the infant who fails to have spontaneous resolution of stenosis must be individualized. Resection with primary anastomosis best serves those infants with limited stenotic lesions, minimal dilatation of the intestinal lumen and no other complicating medical problems. Intestinal diversion with later resection and enterostomy closure should be reserved for infants with intestinal obstruction and complicating medical problems.
BACKGROUND: Prior studies have identified individual risk factors that are associated with necrotizing enterocolitis (NEC); however, the small sample sizes of these previous studies have not allowed the analysis of potential interaction between multiple variables and NEC. Our purpose was to describe the incidence and risk factors for NEC in premature neonates admitted for intensive care. METHODS: We identified neonates as having NEC if they met accepted diagnostic criterion for necrotizing enterocolitis. Using a national database, we assessed the association between NEC and a battery of risk factors previously reported in peer-reviewed literature. RESULTS: There were 15,072 neonates that met inclusion criteria; 14,682 did not have NEC, while 390 (2.6%) met criterion for NEC. Multivariate analysis showed that low birth weight was the most important risk factor for NEC. Other factors that were associated with an increased risk of NEC were exposure to antenatal glucocorticoids, vaginal delivery, need for mechanical ventilator support, exposure to both glucocorticoids and indomethacin during the first week of life, absence of an umbilical arterial catheter, and low Apgar score at 5 minutes. Length of hospital stay and mortality were higher in neonates with NEC than in neonates without NEC. CONCLUSIONS: NEC remains an important cause of morbidity and mortality in prematurely born neonates. In contrast to previous studies, we found that exposure to antenatal glucocorticoids was associated with an increased risk for NEC independent of birth weight.
We investigated the possible role of coagulase-negative staphylococci in necrotizing enterocolitis. Stool coagulase-negative staphylococci isolated from neonates during an outbreak of rotavirus-associated necrotizing enterocolitis were analyzed by a variety of techniques, including speciation, semiquantitative culturing, antimicrobial susceptibility, plasmid profiling and cytotoxicity assays. No differences were observed between the coagulase-negative staphylococci of symptomatic babies and those of asymptomatic controls.
BACKGROUND/PURPOSE: Localized intestinal perforation (LP) is thought to be a distinct entity when compared with perforation associated with necrotizing enterocolitis (NEC). Studies have indicated that LP is more amenable to percutaneous drainage and associated with a better outcome. We sought to determine whether LP and NEC could be distinguished based on clinical parameters alone. METHODS: A retrospective review of 40 neonates with gastrointestinal perforations between January 1990 and May 1998 was performed. All had undergone laparotomy and had histologic specimens available for evaluation. RESULTS: Twenty-one neonates had necrotizing enterocolitis (NEC), and 19 had localized perforation (LP) based on histologic criteria. More neonates with LP were exposed to prenatal indomethacin (37% v 5%; P <.05), received intravenous dexamethasone (42% v 10%; P <.05), had umbilical artery catheters (63% v 14%; P <.05), and had a higher white blood cell (WBC) count (27.1 +/- 23.1 v 14.3 +/- 11.5; P <.05). More neonates with NEC had pneumatosis intestinalis (47% v 11%; P <.05). No significant differences existed in enteral feeding (16% LP v 38% NEC) or overall mortality rate (37% LP v 38% NEC). No statistical differences in the timing of perforation or clinical presentation were found. CONCLUSIONS: NEC and LP are difficult to distinguish based on clinical parameters alone. The authors did find associations between LP and prenatal indomethacin, intravenous dexamethasone, umbilical artery catheters, and a higher WBC count. Mortality rate and clinical outcome were nearly identical in both groups. Pneumatosis intestinalis, thought to be pathognomonic for NEC, was seen on abdominal radiograph in 2 babies with histologically proven LP.
A prospective investigation was conducted to determine if infants with necrotizing enterocolitis had evidence of carbohydrate intolerance prior to the onset of clinical symptoms of advanced disease. Stool specimens were examined for fecal reducing substances with Clintest tablets from well, full-term infants and sick premature infants. Only two of 45 (4.4%) formula-fed, full-term infants demonstrated higher than 2+ fecal reducing substances. Ten of 14 (71%) formula-fed premature infants who developed necrotizing enterocolitis had higher than 2+ reducing substances detected in their stools. Daily measurement of fecal reducing substances can be a useful adjunct in the management of sick premature infants.